Diabetic macroangiopathy: Pathological changes of intracranial arteries in cerebral infarction

Duplication and accessory of the middle cerebral artery (MCA) constitute a rare congenital variation. MCA anomalies are found at a lesser frequency than the vascular anomalies of the other major intracranial arteries. Duplicated/accessory MCA was usually noted incidentally with subarachnoid hemorrhage, due to resulted aneurysmal formation. However, duplicated/accessory MCA-related cerebral infarction is rarer. We report two cases of cerebral infarction due to dissection at the entry of the duplicate/accessory MCA. Both cases were similar in dissected site and clinical course, without headache or injury. In 20 previously reported cases and our two cases of duplicated/accessory MCA-related infarction, mean age (55.8 ± 21.2 years) was slightly younger for cerebral infarction, and stroke etiology was mainly embolism. The main etiologies of stroke were embolism and dissection. Considering embolism etiology, proximal site of arterial diameter changing lesion was a common site for embolism, as duplicated/accessory MCA was usually smaller than normal M1 segment. In cerebral dissection cases, the dissected site was similar to our cases. Numerous mechanisms of dissection were considered, but they mainly included dysfunction of the media and endothelium or shearing stress at the entry of duplication. As the detailed mechanisms of cerebral dissection remain unknown, clinicians should include a differential diagnosis for MCA dissection.

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Experimental study on the pathogenesis of cerebral infarction in rabbits by injecting sephadex G-75 (Part 1). Hourly pathological changes of cerebral tissue due to ischemia.

Nosotchu ◽

10.3995/jstroke.11.337 ◽

1989 ◽

Vol 11 (4) ◽

pp. 337-346 ◽

Cited By ~ 3

Author(s):

Takemichi Kanazawa ◽

Cui De Hua ◽

Osamu Komatsu ◽

Kogo Onodera ◽

Yasaburo Oike

Keyword(s):

Experimental Study ◽

Cerebral Infarction ◽

Pathological Changes ◽

Cerebral Tissue

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Delayed Cerebral Infarction is Systematically Associated with a Cerebral Vasospasm of Large Intracranial Arteries

Neurosurgery ◽

10.1093/neuros/nyz340 ◽

2019 ◽

Cited By ~ 1

Author(s):

Jonathan Brami ◽

Benjamin Chousterman ◽

Grégoire Boulouis ◽

Matthieu Le Dorze ◽

Melinda Majlath ◽

...

Keyword(s):

Computed Tomography ◽

Cerebral Infarction ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Large Artery ◽

Dependent Manner ◽

Imaging Data ◽

Intracranial Arteries ◽

Dose Dependent ◽

Distal Artery

Abstract BACKGROUND Whether delayed cerebral infarction (DCIn) after aneurysmal subarachnoid hemorrhage (aSAH) is driven by large artery vasospasm is still controversial. OBJECTIVE To study the association between DCIn and vasospasm by using quantitative assessment of vasospasm up to distal arteries with time and territorial-based correlation. METHODS Clinical and imaging data of 392 patients with aSAH treated at our center between 2012 and 2017 were reviewed. DCIn was defined as any cerebral infarction occurring within 3 to 21 d after ictus and not related to other specific cause. In patients with DCIn, vasospasm was assessed within 24 h around DCIn for each cerebral artery up to the end of the 2nd segments. DCIn and vasospasm analyses were blinded. RESULTS DCIn was found in 11% of patients (inter-rater k = 0.90, computed tomography (CT)-scan = 100%, follow-up MRI = 91%). Vasospasm was quantified in 258 artery territories including 66 with and 192 without DCIn (DSA = 93%, computed tomography angiography = 7%). Vasospasm was more severe in DCIn than in non-DCIn territories (60% [55-69] vs 20% [0-50], P < .001). Vasospasm was associated with DCIn in a “dose-dependent” manner (P for trend = .022). Every DCIn territory had a vasospasm ≥ 50%, including 39% only of distal artery segments. Only 9% of non-DCIn territories had vasospasm ≥ vasospasm in DCIn territories. CONCLUSION The necessary association between severe vasospasm and DCIn in our study brings additional arguments in favor of large artery vasospasm (especially of distal segments) as a major determinant of DCIn and a potential therapeutic target.

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Experimental Cerebral Infarction. I. Selective Segmental Occlusion of Intracranial Arteries in the Dog

Stroke ◽

10.1161/01.str.1.4.224 ◽

1970 ◽

Vol 1 (4) ◽

pp. 224-237 ◽

Cited By ~ 37

Author(s):

GAETANO F. MOLINARI

Keyword(s):

Cerebral Infarction ◽

Intracranial Arteries ◽

Experimental Cerebral Infarction

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Reversal of cardiomyopathy resulting from prenatal exposure to ethanol

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100113469 ◽

1984 ◽

Vol 42 ◽

pp. 716-717

Author(s):

C. Uphoff ◽

C. Nyquist-Battie

Keyword(s):

Prenatal Exposure ◽

Heart Development ◽

Membrane Integrity ◽

Ethanol Exposure ◽

Prenatal Ethanol Exposure ◽

Pathological Changes ◽

Prenatally Exposed ◽

Inner Mitochondrial Membrane ◽

Fetal Alcohol ◽

Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

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